In this study we investigated the role of the low‐affinity receptor for IgE (FcϵRII, CD23) on Epstein‐Barr virus (EBV)‐transformed human B cells in the uptake and presentation to T cells of antigen after complexing with IgE. Cloned EBV‐transformed B cells were incubated for 5 h with (4‐hydroxy‐3‐iodo‐5‐nitrophenyl)acetyl (NIP)‐haptenized tetanus toxoid (NIP‐TT) or NIP‐TT complexed with a chimeric human IgE/mouse anti‐NIP monoclonal antibody (IgE × NIP‐TT) and then contacted for 2 min with autologous cloned TT‐specific T cells. Intracellular Ca²⁺ mobilization in T cells was determined as an early indicator of T cell activation. The antigen‐presenting capacity of B cells was significantly increased by complexing the antigen with IgE. This effect could be selectively reversed in a dose‐dependent manner by blocking the FcϵRII with an anti‐CD23 monoclonal antibody. The IgE‐mediated increased capacity for presenting antigen became particularly evident when B cells were incubated with NIP‐TT or IgE × NIP‐TT for only 1 h at 4 °C, washed and then cultivated for 6 h at 37 °C allowing uptake and processing of the antigen. These results indicate a new role of the FcϵRII/CD23 molecules in the uptake of antigen by APC which might be of importance in the maintenance of an ongoing immune response against allergens.